Summary of Work: Work has progressed in two major areas: (1) models for human fertility; and (2) statistical methods for monitoring and studying the causes of birth defects. In the first area, we have adapted our fertility model to trials where a method of contraception is evaluated. In other work, we are developing a method to take into account possible errors in identification of the day of ovulation, when estimating fertility parameters. This will allow us to correct for such errors, and thus correct for the artifactual lengthening they cause in the apparent fertile interval. The birth defect work is in its early stages. Case- control studies aimed at elucidating genetic contributors to the etiology of birth defects are problematic because of the "admixture" problem: If a particular variant allele is to be studied, there may be subpopulations that simultaneously have elevated prevalence of the variant and increased risk of the defect, for unrelated reasons. Also, controls may resist genotyping. The case-parents design we propose avoids both these issues by only genotyping cases and their parents. Using the genetic "triad" data from such a study, under assumed Mendelian inheritance, one can estimate relative risks for the allelic variant and can differentiate effects that depend on the maternal genotype from effects that depend on the (correlated) fetal genotype. Simulations reveal that, with such a design, 100 case families will yield a power of >90% to detect a relative risk (dominance model) of 3.0. Extensions will allow for synergistic effects of genotype and an environmental exposure.